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Purpose This prospective study aims to characterize the relationship between binocular summation (BiS) and binocular inhibition (BI) on the quality of life (QoL) of adult and pediatric patients with strabismus. Methods A binocular summation score was measured using ETDRS and Sloan low contrast acuity (LCA) protocols at 2.5% and 1.25% contrast. Patients were categorized as having BiS (binocular visual acuity superior than better-eye visual acuity by 5 or more letters), BI (binocular visual acuity worse than better-eye visual acuity by 5 or more letters) or otherwise indeterminate (less than 5 letter difference between binocular visual acuity and monocular visual acuity of the better-eye). QoL was evaluated by the National-Eye-Institute-Visual-Functioning-Questionnaire-25 (NEI-VFQ-25), 20-item- Adult-Strabismus-Questionnaire (AS-20) and the Amblyopia-and-Strabismus-Questionnaire. Results There was no significant BiS or BI for high-contrast-ETDRS or 2.5% LCA tests. However, mean binocular summation score of −2.14±7.0 letters for 1.25% LCA demonstrated significant binocular inhibition (p=0.004) for this contrast level. Mean composite NEI-VFQ-25 score was significantly lower in subjects with BI on ETDRS (80±19 vs. 57±7 for subjects with BiS and BI, respectively, p=0.03), 2.5% LCA (81±14 vs. 66±16 for subjects with BiS and BI, respectively, p=0.01), and 1.25% LCA tests (91±9 vs. 72±14 for subjects with BiS and BI, respectively, p=0.005). After accounting for potential covariates, significant association persisted for BI demonstrated by 1.25% LCA (p=0.01). With BI demonstrable at 2.5%, AS-20 scores were also significantly lower (p=0.04). Conclusion Strabismic patients with BI had significantly lower QoL scores than those who did not, even after accounting for potential covariates, and even in the absence of diplopia.

Macular microcysts have been associated with various forms of optic atrophy, including neuromyelitis optica. Spectral domain and en face OCT imaging of the microcysts demonstrated a very characteristic pattern. Normal fluorescein and OCT angiography suggest that nonvascular causes, such as Müller cell degeneration, might contribute to the etiologic mechanism.

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